{"id":1314354,"date":"2022-03-12T12:04:14","date_gmt":"2022-03-12T11:04:14","guid":{"rendered":"https:\/\/staging.laboklin.com\/int\/en\/?p=1314354"},"modified":"2024-07-22T13:39:09","modified_gmt":"2024-07-22T11:39:09","slug":"urine-electrophoresis-as-a-useful-tool-for-the-differentiation-of-proteinuria-in-dogs-and-cats","status":"publish","type":"post","link":"https:\/\/laboklin.com\/en\/urine-electrophoresis-as-a-useful-tool-for-the-differentiation-of-proteinuria-in-dogs-and-cats\/","title":{"rendered":"Urine electrophoresis as a useful tool for the differentiation of proteinuria in dogs and cats"},"content":{"rendered":"

[vc_row][vc_column width=”2\/3″][vc_column_text]In dogs and cats, increased urinary protein excretion is pathological and highly correlated with reduced survival of the respective animal. The excretion of small quantities of albumin < 1 mg\/dl is considered physiological in dogs and cats.<\/p>\n

A urine protein-creatinine ratio (UP\/C) of > 0.4 in cats and > 0.5 in dogs is defined as proteinuria according to the guidelines of the IRIS (International Renal Interest Society). A distinction is made between prerenal, renal and postrenal proteinuria. Their various causes are shown in Table 1<\/strong>.<\/p>\n

Urine protein electrophoresis has proven to be a useful tool to differentiate proteinuria. Here, the diluted urine is placed on a gel, the proteins are separated according to molecular weight and it is then possible to distinguish the type of proteinuria from the protein pattern.<\/p>\n

Prerenal proteinuria<\/h2>\n

The excretion of light-chain antibody fragments, so-called Bence Jones proteins, indicates highly pathological prerenal proteinuria. They are produced if multiple myeloma is present and usually cause high-grade proteinuria.
\nIn urine electrophoresis, the patterns of kappa monomers (25 kDa) and lambda dimers (50 kDa) are depicted (Fig. 1<\/strong>). Other common causes of prerenal proteinuria are hypertension, hyperadrenocorticism in dogs and hyperthyroidism in cats.<\/p>\n

Tab. 1:<\/strong> Proteinuria: possible causes and diseases (according to: Harley and Langston, 2012)<\/em><\/p>\n\n\n\n\n\n\n
\u00a0<\/strong><\/td>\ncat<\/strong><\/td>\ncat & dog<\/strong><\/td>\ndog<\/strong><\/td>\n<\/tr>\n
prerenal<\/strong><\/td>\nhyperthyroidism<\/td>\nmultiple myeloma
\nsystemic hypertension
\ndrug reactions
\nacute pancreatitis<\/td>\n		hyperadrenocorticism<\/td>\n<\/tr>\n
renal<\/strong><\/td>\nhyperthyroidism<\/p>\n

 <\/p>\n

any severe inflammatory neoplasia, infectious and immune-mediated disease<\/td>\n

acute renal failure
\nchronic kidney disease
\nglomerulopathy<\/strong>
\nacute pancreatitis
\nviral disease
\ndrug reactions
\nsystemic hypertension
\nDiabetes mellitus
\nendocarditis<\/td>\n		hyperadrenocorticism<\/p>\n

 <\/p>\n

immune-mediated disease (systemic lupus erythematosus, immune-mediated haemolytic anaemia,
\npolyarthritis, hepatitis)
\nleptospirosis
\nheartworm disease<\/td>\n<\/tr>\n

postrenal<\/strong><\/td>\n\u00a0<\/strong><\/td>\nlower urinary tract disease
\nreproductive tract disease<\/td>\n		<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

 <\/p>\n

Renal proteinuria<\/h2>\n

For one, this includes glomerulopathies in which high molecular weight proteins larger than albumin (> 70 kDa) can no longer be retained by the glomerular apparatus due to various defects.<\/p>\n

Glomerulopathies are associated with a variety of infectious (e.\u00a0g. ehrlichiosis, babesiosis and leishmaniasis in dogs; FIV, FELV and FIP in cats), neoplastic, parasitic, autoimmune and endocrine causes.<\/p>\n

Furthermore, we distinguish tubulopathies in which the capacity or ability of the proximal tubule to reabsorb low molecular weight proteins (< 70 kDa) is exhausted.<\/p>\n

These tubulopathies manifest as Fanconi syndrome in dogs, which is hereditary in Basenjis and caused by toxic factors in other breeds, e.\u00a0g. after the administration of gentamicin (Fig. 2<\/strong>).<\/p>\n

Mixed proteinuria, in which both protein groups can be detected, mainly occurs in stages 2 \u2013 4 of chronic kidney disease and in acute kidney injury because, in addition to glomerular dysfunction, it also causes renal tubular acidosis (Fig. 3<\/strong>).<\/p>\n

Since treatment of proteinuria can vary greatly depending on the cause, it is essential to determine whether renal proteinuria is glomerular, tubular or mixed glomerular-tubular proteinuria.<\/p>\n

Postrenal proteinuria<\/h2>\n

This is usually caused by lower urinary tract and reproductive tract disease, can be detected by examination of urine sediment and does not require differentiation by urine electrophoresis.[\/vc_column_text][\/vc_column][vc_column width=”1\/3″][vc_column_text]<\/p>\n\n\t\t\t